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Biomedical subjects

R B Philp

Publications and source records attributed to R B Philp.

At least 55 records · Page 3Linked to original sources
PubMed1979

Changes in platelet function and gastrointestinal bleeding following repeated administration of acetylsalicylic acid in the rat and the dog.

Two dogs were prepared with Pavlov pouches of the fundic area of the stomach using standard techniques. During treatment periods of 14 days, 200 mg acetylsalicylic acid (ASA) was introduced into the pouch twice daily by insufflation. One hour after each drug administration the pouch was washed with saline and the fluid assayed for blood. Bleeding from the pouch increased to a maximum on the 3rd or 4th day of the treatment period and subsequently declined such that by the 8th day blood loss was minimal and approximated that found during control periods. Platelet aggregation (in vitro) responses to adenosine diphosphate were significantly (p less than 0.01) inhibited on day 3 when aggregation curve heights were reduced by 66.2 +/- 13.11% (mean +/- SEM) from control values. On day 7 and during the ensuing 7-day period when ASA was given twice daily, the heights of aggregation responses were reduced by only 20-30% from controls. These responses were significantly (p less than 0.001) greater than those found on day 3. Similar changes in platelet reactivity were found in plasma from rats given ASA twice daily for 7 days. Aggregation responses to collagen were depressed by 95.5 +/- 4.49% on day 1 following two doses of ASA. As the treatment period continued, the aggregation responses increased in magnitude until the 7th day they were similar in height to those from control animals. The mechanism involved in this adaptation to ASA treatment seen with these platelets is not known.

Adenosine Diphosphate↗
PubMed1979

Effects of aspirin and dipyridamole on platelet function, hematology, and blood chemistry of saturation divers.

Twenty-four young male divers were assigned randomly to 4 treatment groups: Group I received aspirin (325 mg) three times daily; II received dipyridamole (75 mg) three times daily; III received both drug regimens; and IV received matching placebo. Double-blind procedures were followed. Treatment began 24 h prior to a 48-h saturation dive (inclusive of 17 h decompression) at a simulated depth of 18.3 m and continued throughout and for 3 days after the dive. A post-dive reduction in circulating platelet count was observed in all groups, except the group that received aspirin only. Platelet survival was shortened in all treatment groups. Five cases of Type I decompression sickness occurred and were treated by recompression, two in the aspirin plus dipyridamole group, two in the dipyridamole group, and one in the placebo group. Blood chemistry and hematology profiles showed that divers with decompression sickness had more elevated GOT, GPT, CPK, cholesterol and triglyceride levels, and greater reductions in platelet count, Platelet Factor 4 and Thrombin Clotting Time than most other subjects. Subjects receiving either aspirin or aspirin plus dipyridamole had fewer changes in these parameters. Failure of aspirin to potentiate, or add to, dipyridamole may be due to other actions of aspirin such as inhibition of prostacyclin synthesis. Further studies of the role of antiplatelet drugs in decompression sickness are warranted.

Adult↗
PubMed1978

Effect of ibuprofen on platelet function in normal subjects and hemophiliac patients.

New propionic acid derivatives are claimed to induce a lower incidence of gastrointestinal bleeding and hemostatic disturbance than older anti-inflammatory analgesics such as aspirin. One of these (ibuprofen, Motrin) was given (600 mg orally) to normal subjects and hemophiliac subjects on a random, double-blind basis (lactose placebo). Platelet adhesiveness, aggregation, platelet and red cell counts, percent packed cells, percent hemoglobin, serum ibuprofen levels, and modified Ivy bleeding time were measured before and 2 and 24 hr after drug. Predrug and 24-hr postdrug values were normal, but at 2 hr after drug, adenosine diphosphate, epinephrine, and collagen aggregations were inhibited and bleeding times were slightly but significantly prolonged in the ibuprofen-treated normal subjects. The other parameters tested remained unchanged. Similar results were obtained in the ibuprofen-treated hemophiliac patients, although bleeding time was not prolonged. The results suggest that ibuprofen may be given to hemophiliac subjects with greater safety than some of the older anti-inflammatory drugs.

Adolescent↗
PubMed1978

Comparison of antithrombotic activity of heparin, ASA, sulfinpyrazone and VK 744 in a rat model of arterial thrombosis.

Rat carotid arteries were injured electrically (350 V, 2 mA DC for 5 min) before and after the intravenous administration of heparin (1,000 U/kg), VK 744 (25, 50, 100 mg/kg) ASA (100, 200 mg/kg) and sulfinpyrazone (50, 100, 150, 200 mg/kg). Thrombus growth was quantified by recording arterial temperature change distal to the injury. Heparin completely blocked thrombus formation in most experiments. All other agents exhibited antithrombotic activity with sulfinpyrazone being most potent. None was as effective as heparin. This model may be a useful tool for screening antithrombotic drugs.

Animals↗
PubMed1976

Changes in blood enzyme activity and hematology of rats with decompression sickness.

Plasma activities of lactic dehydrogenase (LDH), creatine phosphokinase (CPK), glutamic pyruvic transaminase (GPT), and alkaline phosphatase (ALP) were studied, along with hematological changes, in rats suffering from various degrees of experimental decompression sickness (DS). By 1 h after decompression, LDH and CPK activities were elevated in moderate and severe DS whereas GOT and GPT were elevated only in severe DS. ALP was reduced in all decompressed rats. Hematological changes indicated hemoconcentration, the degree of which paralleled the severity of DS. By 24 h after decompression, all enzyme activities were approaching control levels with the exception of GOT, which was further elevated from the 1-h value. The observed lung damage in rats with severe DS in conjunction with the hematologic and enzyme data suggested that hypoxemic-hypoxia, incident to bubble embolization of pulmonary vasculature, was a major factor in altering the blood enzyme pattern in DS. Serum enzyme data from two inadequately decompressed divers are also reported.

Alanine Transaminase↗
PubMed1975

Hematology and blood chemistry in saturation diving: I. Antiplatelet drugs, aspirin, and VK744.

Blood chemistry and cellular parameters were studied before, during, and after saturation (2.4 ATA) dives in the HYDRO-LAB habitat on two separate occasions. In both, platelet count fell greater than 20% 12-24 hours after surfacing and moderate (5%) reductions in hemoglobin, red-cell count, and packed-cell volume were observed. Plasma cholesterol and triglyceride levels were depressed postdive as were most plasma enzymes (GOT, GPT, CPK, LDH, ALP). The latter changes were very slight. In the first study, the incidental ingestion of aspirin by some divers did not prevent the loss of platelets even though the platelet-release reaction in response to ADP was inhibited. In the second study the platelet-suppressive drug VK744 was administered, on a double-blind randomized basis, to six divers, six others taking a placebo capsule. Dosage of VK744 was 300 mg TID for 2 days before, 5 days during, 3 days after saturation dive. The drug inhibited the postdive loss of circulatory platelets and in fact the treated group showed a rebound in platelet count above control values, 48-72 hours postdive. Megathrombocyte counts indicated the production of new platelets in both groups at this point. The treated group also showed a marked and significant reduction in plasma cholesterol and triglycerides, suggesting an antilipidemic effect of the drug. Theses results confirm previous observations and indicate that postdecompression loss of platelets may be related to sequestering of reactive platelets, possibly by microbubbles, and that the phenomenon can be inhibited by some antiplatelet drugs.

Adult↗
PubMed1975

Hematology and blood chemistry in saturation diving: II. Open-sea vs. hyperbaric chamber.

Hematograms, platelet function, and blood-enzyme chemistry were compared in two similar saturation-excursion dives, one conducted in a hyperbaric chamber and the other in the open sea. The chamber dive was more stressful in that it was preceded by a series of bounce decompression dives (one of which produced a 100% incidence of cutaneous pruritus in four subjects) and in that the excursions from saturation depth (60 fsw or 2.818 ATA) were longer and deeper (producing one case of O2 convulsions, one of confirmed decompression sickness, and several of Doppler-detected vascular bubbles). The chamber dive was associated with a marked and significant reduction in circulating platelet count; significant increases in plasma enzyme activities in the victim of O2 toxicity (LDH, CPK) and in one subject with Doppler bubbles and questionable bends symptoms (LDH, GOT, GPT) but not in another; and mild but significant anemia. In the open-water dive, one subject, who developed symptoms of gastroenteritis, showed moderate elevation of LDH, GOT, and GPT activity. No significant change in platelet counts occurred. Both dives were associated with elevated white-cell counts, apparently as a result of numerous minor infections, and reduced sensitivity of platelets of ADP-induced aggregation.

Alanine Transaminase↗